Transcription factor redundancy ensures induction of the antiviral state

J Biol Chem. 2010 Dec 31;285(53):42013-22. doi: 10.1074/jbc.M110.165936. Epub 2010 Oct 13.


The transcriptional response to virus infection is thought to be predominantly induced by interferon (IFN) signaling. Here we demonstrate that, in the absence of IFN signaling, an IFN-like transcriptome is still maintained. This transcriptional activity is mediated from IFN-stimulated response elements (ISREs) that bind to both the IFN-stimulated gene factor 3 (ISGF3) as well as to IFN response factor 7 (IRF7). Through a combination of both in vitro biochemistry and in vivo transcriptional profiling, we have dissected what constitutes IRF-specific, ISGF3-specific, or universal ISREs. Taken together, the data presented here suggest that IRF7 can induce an IFN-like transcriptome in the absence of type-I or -III signaling and therefore provides a level of redundancy to cells to ensure the induction of the antiviral state.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antiviral Agents / chemistry
  • Antiviral Agents / pharmacology*
  • Cell Line, Tumor
  • Gene Expression Regulation*
  • Humans
  • Interferon Regulatory Factor-7 / metabolism*
  • Interferon-Stimulated Gene Factor 3 / metabolism*
  • Interferon-Stimulated Gene Factor 3, gamma Subunit / metabolism*
  • Mice
  • Mice, Transgenic
  • Promoter Regions, Genetic
  • Signal Transduction
  • Transcription Factors / chemistry*
  • Transcription, Genetic


  • Antiviral Agents
  • IRF7 protein, human
  • IRF9 protein, human
  • Interferon Regulatory Factor-7
  • Interferon-Stimulated Gene Factor 3
  • Interferon-Stimulated Gene Factor 3, gamma Subunit
  • Irf7 protein, mouse
  • Transcription Factors